So we've gone back and forth quite a bit on IVC ultrasound these past couple of days:
- iSepsis – Vena Caval Ultrasonography – Just Don't Do It!
- An Uproar about the IVC
- EM Nerd-The Case of the Tarnished Standard
- The IVC for Fluid Assessment Roundup
So it would probably be helpful to have some physiologic basis for all of this. Enter Jon-Emile S. Kenny MD, intensivist and practical physiologist. Here are some words and a video from him:
Guest Post
It is hard to believe that it was 3 years ago when I entered the vibrant and ever-expanding FOAMed community. The ethos of my contribution – heart-lung.org – was, and remains, the provision of lectures and learning modules in detailed physiology germane to the practice of critical care without cost – world-wide. To initially promote heart-lung.org, I wrote a brief piece on the physiology of IVC collapse at pulmccm.org
[http://pulmccm.org/main/2014/critical-care-review/inspiratory-collapse-inferior-vena-cava-telling-us/]
With that post, I had hoped to raise caution on the use of IVC collapse because of its complex physiology; I followed with another entry in early 2016 describing the mechanisms of false positives and false negatives for IVC collapse and detecting fluid responsiveness
[http://pulmccm.org/main/2016/cardiovascular-disease-review/that-fallible-ivc/]
Given the aforementioned, it is with tremendous interest that I read Dr. Marik’s commentary on IVC collapse and subsequent squabbles. Just 2 weeks ago, I was exceptionally honoured to have been invited to speak at the Department of Emergency Medicine Grand Rounds at Mount Sinai Hospital. For that talk, I started animating a slide on the physiology of IVC collapse & dilation, but did not finish it in time for my presentation. I have since finished the animation and would like to share it with you now. What I hope to illustrate clearly is that the relative simplicity of obtaining IVC data in vivo should not belie its complex physiological underpinnings and, therefore, its nuanced interpretation.
The following are pertinent references [1-8] for the animation:
- Corl, K., A.M. Napoli, and F. Gardiner, Bedside sonographic measurement of the inferior vena cava caval index is a poor predictor of fluid responsiveness in emergency department patients. Emerg Med Australas, 2012. 24(5): p. 534-9.
- Corl, K.A., et al., Inferior vena cava collapsibility detects fluid responsiveness among spontaneously breathing critically-ill patients. Journal of Critical Care, 2017. 41: p. 130-137.
- Bodson, L. and A. Vieillard-Baron, Respiratory variation in inferior vena cava diameter: surrogate of central venous pressure or parameter of fluid responsiveness? Let the physiology reply. Crit Care, 2012. 16(6): p. 181.
- Muller, L., et al., Respiratory variations of inferior vena cava diameter to predict fluid responsiveness in spontaneously breathing patients with acute circulatory failure: need for a cautious use. Crit Care, 2012. 16(5): p. R188.
- Magder, S. and F. Bafaqeeh, The clinical role of central venous pressure measurements. J Intensive Care Med, 2007. 22(1): p. 44-51.
- Barbier, C., et al., Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med, 2004. 30(9): p. 1740-6.
- Feissel, M., et al., Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock. Chest, 2001. 119(3): p. 867-73.
- Juhl-Olsen, P., C.A. Frederiksen, and E. Sloth, Ultrasound assessment of inferior vena cava collapsibility is not a valid measure of preload changes during triggered positive pressure ventilation: a controlled cross-over study. Ultraschall Med, 2012. 33(2): p. 152-9.
- EMCrit Guest Post – Bougie Lessons from the Literature and Experience by George Kovacs - January 3, 2020
- Guest Post – The 3D Printed Endobronchial Trainer by Matt Mac Partlin - October 23, 2019
- EMCrit Guest Post – Drawing Circles for Bougie Hangup by Neil Dasgupta - September 6, 2019
Dr Kenny, Your animation does an excellent job in highly the complexity of the IVC collapse (or distension) with multiple factors influencing this “pseudo-parameter”. What interests me is the physiology behind IVC collapse (or distension) rather than the sensitivity or specificity of this “pseudo-parameter” and how this relates to bi-ventricular preload dependency (or not). We all understand (hopefully) the elegance of the physiology behind pulse pressure variation (PPV), and stroke volume variation (SVV) is the sedated patient receiving 8mls/kg positive breaths (i.e in the operating room). Similarly, the physiology behind the passive-leg raising (PLR) maneuver) in determining bi-ventricular preload dependency… Read more »
Hi Dr. Marik. Thank you for your question; it is an excellent question. The relationship is complex, difficult to describe with words and probably best understood using the Guyton Diagram. The animation that I used in the vodcast above is, essentially, a cartoon of Guytonian physiology. The right atrial pressure is formed by the intersection of venous return and cardiac function. Because the right atrial pressure lies at the cross-roads of venous return and cardiac function, the value itself cannot tell us anything definitive about the slope of the cardiac function curve [volume responsiveness] or venous return [partially determined by… Read more »
I like the idea of considering two different physiological issues going on here. To that end could you not consider them individually to guide your treatment decisions? What about comparing RV volume to LV volume to decide if it’s a pump issue. What about considering the slope of the a and v lines of the CVP to reflect the capacitance of the venous system (steeper slopes = more unstressed being converted to stressed). The idea that any one parameter can accurately reflect the function of a multi system problem is what gets us in to trouble. I love this recent… Read more »
I would also like to point out that I still have a hard time rationalizing the idea of giving tremendous amounts of fluids to a patient that hasn’t necessarily lost tremendous amounts of fluid. Just like we have decided that filling hemorrhage patients with blood is better than saline I don’t understand how we think the best way to treat profound vasopalegia is to fill to tank more until we get a pressure that we like. Insensible loss increases from sepsis aside, it’s seems hugely obvious to me that a better way to go would be to convert that vasoplegic… Read more »
You hit the Jackpot.
Thanks so much for your comments and your suggestions. I think that you sum it up perfectly when you say: “The idea that any one parameter can accurately reflect the function of a multi system problem is what gets us in to trouble.” Yeup. I try to look at it simply; you have to test the question that you are asking. If you desire to know if the heart is fluid responsive, you have to 1. augment its preload and 2. rapidly determine if it’s increasing its output in response; for example a passive leg raise with doppler velocity measurement.… Read more »
[…] I was delighted to read Dr. Marik’s very recent take on IVC collapse and thank Scott for posting my vodcast on the topic. The discussion also included a very thoughtful essay by Rory […]
[…] Läs mer: https://emcrit.org/emcrit/physio-ivc-collapse/ […]